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IMS > Blood- blood diseases, haemostasis, role of platelets and coagulation and thrombotic disease > Flashcards

Blood- blood diseases, haemostasis, role of platelets and coagulation and thrombotic disease Flashcards

1
Q

Circulatory system- what do the arteries, veins, articles, venules and capillaries do?

A

Arteries (red-oxygen rich)- brings blood from the heart to the organs and tissues
Veins (blue oxygen poor)- returns blood from organs and tissues to heart, followed by lungs for re-oxygenation
Arterioles, venules, capillaries- small blood vessels in organs/tissue which have a small diameter and thus maximise blood-tissue interaction

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2
Q

Functions of the blood

A
  • Hydration of tissues and organs
  • Delivery of oxygen and nutrients to tissues and organs- how all tissues get metabolic fuels
  • Distribution of (endocrine) hormones- allows for homeostatic balance
  • Fight infection: Innate and adaptive immune responses- blood transports what requires to fight infection
  • Regulation of body temperature (vasoconstriction/vasodilation) and pH- ensures blood doesn’t become too alkaline/acidic by having a buffering system
  • To prevent its own (blood) loss
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3
Q

What does the erythrocyte do?

A

The most abundant blood cell is the erythrocyte, which has oxygen transport as its main function.
NO NUCLEUS OR MITOCHONDRIA.

Erythrocytes contain haemoglobin which regulates oxygen transport

Delivery of life supporting material glucose, amino acid, fatty acids, vitamins, minerals. – required for metabolic processes and proteins
Deliver regulating signals, i.e., hormones to tissue cells
Collect waste products from tissue cells and deliver to special organs (kidney, lung) for disposal
Distribute heat throughout the body

No mitochondria- doesn’t use oxygen so energy comes through anaerobic glycolysis.
Cytoskeleton made of spectrin so allows cells to change shape/ fold half so can squeeze through capillaries.

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4
Q

What blood cells fight infection and allergic reactions?

A

White blood cells contribute to the immune response against infection (all white cells) and to allergic reactions (eosinophils and basophils).

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5
Q

How is the blood involved in hormone distribution?

A
  • Endocrine hormones are secreted by endocrine glands directly into the blood to be circulated to remote target tissues
  • Paracrine hormones have target cells within the tissue that secreted the hormone
  • Endocrine hormones include – oestrogen, insulin, thyroid stimulating hormone, vasopressin and adrenalin
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6
Q

How is blood loss prevented?

A

Haemostasis

Platelets- small anucleate blood cells that clump together

Blood coagulation pathway- through formation of thrombin a fibrin clot is formed

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7
Q

How are there different blood cells?

A

All blood cells derived from one common progenitor cell in the bone marrow- the multipotential haematopoietic stem cell

Multipotential (can create different type of cells) haematopoietic (producing cells going into the blood) stem cell.

Two major lineages: myeloid and lymphoid, these produce 11 different types of blood cell

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8
Q

Composition of blood- blood plasma

A

Blood plasma (55% blood volume) contains components of the blood coagulation (clotting) and immune (fighting infection) systems, metabolites and proteins.

Most abundant blood plasma proteins :

  1. Albumin (35-50 g/L), “filler” -60/70% of blood- contributes to the osmotic pressure of the blood and a critical transporter when things aren’t soluble in blood e.g. fatty acid which can be transported now
  2. Immunoglobulins (15 g/L), involved in fighting infection
  3. Fibrinogen (3-5 g/L), involved in clotting- clotting process goes over board to ensure enough fibrinogen to clot

Plasma= Serum+ clotting factors (+clotting inhibitor)

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9
Q

Composition of blood-blood serum

A

Blood serum similar to blood plasma but is allowed to clot before centrifuged.

Serum= Plasma- clotting factors

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10
Q

ABO blood groups

A

Blood group A (42%)- has A antigens on the red blood cells with anti-B antibodies in the plasma
Blood group B (10%)-has B antigens with anti-A antibodies in the plasma
Blood group O (44%)-has no antigens, but both anti-A and anti-B antibodies in the plasma
Blood group AB (4%)- has both A and B antigens, but no antibodies

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11
Q

Agglutinin

A

Agglutinin- an antibody that causes agglutinogen. B against B agglutiongens, same with A

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12
Q

Agglutinogen

A

Agglutinogen- antigenic substance in blood cells which stimulates agglutinin in blood serum

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13
Q

Function of agglutination

A
  • Bind to agglutinogens that aren’t carried by host RBCs

* Cause agglutination aggregation and lysis of incompatible RBC

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14
Q

RBC vs plasma compatibility by ABO blood group

A

Blood plasma- antibodies that are in the blood rather than the cells themselves

AB no antibodies so can give to anything, A and B have antibodies, O have both antibodies for A and B so can receive from all.

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15
Q

What happens if patient given wrong blood group?

A

If transfusion wrong- haemolysis- blocking of blood cells and make tissues hypoxic.

  • Lysis of RBC so get haemoglobin and iron in blood get into kidneys and get kidney failure.
  • Hypotension (low BP)
  • Bleeding-all clotting system used and can’t produce enough so start bleeding.
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16
Q

Rhesus (Rh) blood groups

A

channel antigen on the RBC membrane- D antigen

• Rh+ (common) and Rh- (rare)

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17
Q

Haemolytic syndrome in the foetus/new born

A

Women at the moment rhesus negative, child rhesus positive-not issue as placenta separating.

Tearing of placenta can causes positive and negative mix and mother produces antibodies so immunizes mother.

Second pregnancy- antibodies start clotting and baby born with severe anemia.

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18
Q

Diseases of Blood Plasma

A

Bleeding, Thrombosis, Hereditary angioedema, Complement deficiency

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19
Q

Diseases of Blood Cells

A

Haematological malignancies, Sickle Cell Anaemia, Thalassaemia, Haemoglobinopathies, Leukopenia, Thrombocytopenia and infectious mononucleosis

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20
Q

What is bleeding caused by?

A

May be caused by
– Injury (acute)
– Disease (chronic)- e.g. constantly bleeding ulcer
– Low platelet counts (thrombocytopenia - mild)
– Coagulation deficiencies (haemophilia - severe)
– Vitamin K deficiency- required to produce coagulation factors
– Drugs
– Liver disease (although may also cause thrombosis)- produces clotting factors thus reduction of clotting factors
– Infection/sepsis: disseminated intravascular coagulation- all coagulation
– Aneurysm rupture

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21
Q

Which blood disorders cause the number of blood cells to decrease?

A
  • Decreased number of RBC called anaemia
  • Decreased number of WBC called leukopenia
  • Decreased number of platelets called theombocytopenia
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22
Q

Which blood disorders cause the numbers of blood cells to increase?

A
  • Increased number of RBC called erythrocytosis
  • Increased number of WBC called leukocytosis
  • Increased number of platelets called thrombocytosis or thrombocythemia
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23
Q

What is thrombosis and what is it caused by?

A

Thrombosis- local coagulation or clotting of the blood in a part of the circulatory system

Caused by:
• Atherosclerosis- lipids position in the arterial walls to form atherosclerotic plaque
• Cancer
• Immobilisation- not moving for a long time so pooling of blood in lower extremities
• Surgery
• Hypercoagulability
– Inhibitor (PC, PS, AT) deficiencies
• Thrombocythaemia (high platelets level)
• Factor V Leiden

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24
Q

How are haematological malignancies classed?

A

• Classified according to blood cell lineage
– Myeloid neoplasm
– Lymphoid neoplasm
• And according to location
– Leukaemia (blood)-myeloid
– Lymphoma (lymph nodes)-lymphoid
• Acute (weeks – blasts) or chronic (years – mature cells)
• Many subtypes
• Disease are categorised as myeloid or lymphoid disorder

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25
Q

Neoplasia

A

• Uncontrolled cell growth
• Two classes of genes implicated
-Oncogenes: directly causative of cancer – includes growth factors and their receptors, DNA binding proteins- genes that regulate cells/cell cycle- if become mutated become oncogenes
-Tumour suppressor genes: loss of suppressor activity leads to cancer

Cancer may be initiated by:
• Point mutations (UV light, radiation, carcinogens)
• Chromosome translocation
• Viral genes- retroviruses

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26
Q

What is anaemia? What are the symptoms?

How is it caused?

A

Loss of oxygen delivery, Hb levels are low.

Symptoms are Tiredness, Pallor, Fainting, tachycardia, Shortness of breath

Caused by abnormalities in:

  • RBC or haemoglobin production- not enough
  • RBC destruction (been produced but have been destroyed)
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27
Q

Decreased response to erythropoietin- Iron-Deficiency

A

Iron is an essential element of the haem group in haemoglobin. Leads to microcytic anaemia (pale and small RBCs) due to reduced haemoglobin production.

Causes:

  • Diet induced
  • Blood loss (acute or chronic)
  • Infection (hookworm)
  • Growth spurts (children), pregnancy
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28
Q

Decreased response to erythropoietin- Vit B12 or folate deficency

A
  • Vit B12 and folate involved in DNA replication
  • Deficiency of either causes problems with mitosis (cell division) of the proerythroblast
  • This causes megaloblastic or macrocytic anaemia (large RBCs)
  • Vit B12 deficiency mostly caused by reduced absorption
  • Folate deficiency may be caused by poor nutrition, alcoholism (can’t be bothered to eat as they prefer to drink), malabsorption, certain drugs
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29
Q

What does EPO do?

A

EPO is produced by interstitial fibroblasts in the kidney. Renal disease can lead to anaemia. Recombinant EPO is therapeutic for renal disease induced anaemia.

Tissue becomes anoxic. Kidney sense hypoxia and release EPO, goes to the marrow and starts producing more RBC (erythropoiesis) feeds back to kidney and now switches off EPO. Never switches off though as always high/low production.

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30
Q

Haemolytic anaemia

A
  • Due to increased RBC destruction
  • Bone marrow unable to replace sufficient RBCs
  • Acquired (malaria, sepsis)
  • Inherited (G6P dehydrogenase, Autoimmune Hemolytic Anemia)
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31
Q

Acquired haemolytic anaemia

A 
•	Immune 
–	Haemolytic syndrome in the newborn (Rh)
–	Autoantibodies
–	Complement system
•	Non-immune
–	Drug-induced
–	Snake venom
–	Mechanical (heart valves)
–	Infections (malaria, septicaemia)
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32
Q

Inherited haemolytic anaemia

A

Virtually all inherited anaemias are haemolytic

  1. RBC cytoskeletal defects
  2. RBC enzyme defects
  3. Haemoglobin defects
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33
Q

What are the causes and effect of sickle cell disease?

A

Cause:
• Mutation in the Hb B globin gene Glu 6Val
• Polymerisation of Hb, distorting RBC
• Widespread in Africa (Carribean), Middle East, India and Med

Effect:
• “Sickling” of RBC (particularly in homozygous disease)
• Sickle cell crisis due to blockage of microvasculature
• Heterozygosity confers protection against malaria- why prevalent in Africa and Asia

34
Q

Causes of thalassemia

A
  • Common in Africa, Middle East, Asia and the Med
  • Mild in heterozygous form, protection against malaria
  • Alpha thalassaemia – deletions of alpha globin
  • Beta thalassaemia – point mutations in the B globin gene, both copies of the gene affected the patient has HbF (foetal haemoglobin) and beta thalassaemia major
35
Q

Haemostasis

A

Haemostasis- process that maintains the flowing blood in a fluid state and confined to the circulatory system

36
Q

Hemorrhage

A

The process of bleeding

37
Q

Thrombosis

A

The process of clotting

38
Q

Fibrinolysis

A

The process of clot dissolution

39
Q

Haemostatic strategy

A

The haemostatic mechanism is not a single biological pathway, but the product of the complex interactions of a normal of distinct systems:

  • the blood vessels- barrier to stop blood escaping but releases chemicals to ensure blood stays fluid
  • blood platelets
  • blood coagulation system
  • blood fibrinolytic system
  • inhibitors of the above
40
Q

Primary response

A

Platelet-mediated
Endothelial-mediated
Fibrinogen-mediated

41
Q

Secondary response

A

Circulating enzymes
Platelet mediated
Fibrin mediated

42
Q

Haemostasis- process

A
  • Once cut ourselves, collagen flows to the blood and initiates a reaction. Catches and causes platelets to stick- adhesion
  • Platelets activated attract more platelets by secreting chemicals
  • Aggregation by fibrinogen – easy to wash away
  • This is the primary response
  • Coagulation cascade convert fibrinogen to fibrin and then will be difficult to break down so it is hard to wash away
43
Q

Localisation of haemostatic response

A
  • Only activated when exposed to collagen, when you cut yourself
  • Coagulation cascade can’t occur without platelets so keeps it all in one place
  • Clot can break off (embolism)
44
Q

How do platelets respond rapidly to vascular injury?

A

Platelets circulate in a quiescent (inactive) state but undergo an “explosive” activation when they encounter vascular injury.

  • Large number of receptors- interact with other cells
  • High number of platelets
  • Rich in signaling proteins- send autocrine and paracrine messages to allow rapid reponse
  • Positive feedback
45
Q

Haemostasis and thrombosis- primary response

A

Blood platelets- platelet adhesion and spreading

  1. Platelets bind to exposed collagen
  2. Shape change
  3. Release granules- agents drive platelet activation
  4. Recruitment
  5. Aggregation
46
Q

What is limited proteolysis?

A
  • Proteolysis – protein cut into smaller fragments usually by hydrolysis of peptide bonds by enzymes such as trypsin
  • Limited proteolysis by coagulation factors is much more specific – one protein, one cut
  • Induces conformational change
47
Q

Blood platelet structure

A

Anucleate. Life span 7-10 days

When activated by collagen changes shape (sticks arms out) to get hold of platelets.

48
Q

Primary haemostasis- reaction to vascular trauma

A

• Vasoconstriction, reduction of blood flow to the area
• Platelet activation and adhesion to collagen
• Platelet shape change
• Granule release – increased local concentrations of
platelet activators
coagulation factors
vasoconstrictors
• acts to amplify the haemostatic response
• primary plug formed and blood loss stopped

49
Q

Importance of localisaiton

A
  • Ensure blood is fluid- don’t want clotting so blood vessels blocked
  • Platelets only activated when they see collagen
  • Platelets need to stick together by fibrinogen cant bind by fibrinogen unless they’ve bound to collagen- stops interaction away from site injury
  • Platelet plug not that strong, enzyme thrombin does this but doesn’t want it floating around. Proteins that drive thrombin generation are localised and only activated at surface of platelet which is at the site of injury
  • Thrombin escapes, inhibitors inhibit it and dilute it down
50
Q

Secondary haemostasis- consolidation of the haemostatic plug

A

Coagulation initiated by 4 steps.

Coagulation is triggered by exposure of the blood to tissue factor (TF). TF is a transmembrane (receptor) protein expressed on perivascular cells (cells surrounding the blood vessel), such as fibroblasts and smooth muscle cells. Certain organs such as the brain are particularly rich in TF.

1) After injury, FVII from the blood binds to TF expressed on the membrane of cells surrounding the blood vessel
2) FVII is a peculiar clotting factor in that it shows auto-activation. Activated FVII next proteolytically cleaves and activates FX.
3) FXa then converts prothrombin to thrombin and thrombin (on platelet surface).
4) Converts fibrinogen (on platelet surface) to fibrin.

51
Q

Followed by additional reactions to consolidate (enhance) thrombin generation- extrinsic pathway

A
  1. Coagulation triggered by exposure of tissue factor (transmembrane receptor protein) to FVII
  2. aFVII cleaves and activates FX to FXa which coverts prothrombin to thrombin
  3. thrombin converts fibrinogen to fibrin – HOWEVER NOT ENOUGH THROMBIN FOR NOMAL HAEMOSTATIC RESPONSE, corroborated by intrinsic pathway
52
Q

Followed by additional reactions to consolidate (enhance) thrombin generation- intrinsic pathway

A
  1. triggered by contact with a negatively charged non-endothelial surface – glass, silica, collagen
  2. activation of FIX by FVIIa/TF to FIXa (can then convert FX to FXa)
  3. activation of FXI, FVIII and FV by thrombin (FVIII and FV are cofactors for FIXa and FXa)
53
Q

Difference between major and minor bleeds

A

Major bleeds require treatment- plasma, platelets, coagulation factor concentrates
External-trauma, surgery
Internal- haemophilia (joint/muscle), aneurysm rupture, drug-induced, gastro-intestinal

Minor bleeds don’t require treatment- Normal bruises, menorrhagia, epistaxis

54
Q

Bleeding disorders can be induced or inherited

A
  • Induced (acquired)- trauma, surgery, infection and other disease
  • Inherited/spontaneous- no obvious cause and likely caused by congenital (coagulopathy) disorder
55
Q

What does sepsis cause?

A

Sepsis causes a disorder called disseminated intravascular coagulation (DIC). Tissue factor is the major driver of coagulation.

Infection leads to Sepsis leads to Tissue Factor Exposure leads to systemic coagulation activation leads to microvascular clots/consumption of clotting factors and platelets leads to bleeding leads to multiple organ failure

56
Q

Disseminated intravascular coagulation (DIC)

A

An acquired syndrome characterized by the intravascular activation of coagulation with loss of localisation arising from different causes

Typically originates in the microvasculature, leads to organ dysfunction. Coagulation cascade (especially thrombin) is activated inappropriately.

Coagulation factors are consumed at a rate in excess of the capacity of the liver to synthesize them.

Not enough coagulation factors to stop bleeding.
Platelets are consumed in excess of the capacity of bone marrow megakaryocytes to release them.

57
Q

Abdominal aortic aneurysm (AAA)

A
  • Progressive dilatation of the abdominal aorta inferior to the renal and above the iliac arteries
  • More common in men
  • High risk of rupture if aneurysm becomes too large
  • AAA Rupture associated with major internal bleeding and 50% mortality
58
Q

The importance of Vitamin K

A

Vitamin K is a cofactor for an enzyme, enzymes takes glutamic acid and adds it to the factors.
Without reaction taking place, these factors are ineffective as cant be bound to platelet surface during coagulation response. Vitamin K is a fat soluble vitamin and is not synthesised so taken through diet.

59
Q

Causes of Vitamin K deficency

A
  • Malnutrition
  • Fat malabsorption
  • Liver disease (alcoholic cirrhosis)
  • May occur in newborns (vitamin K injection/tablets for newborns)
  • Due to Vitamin K Antagonists (VKA: warfarin, acenocoumarol) over-dosage
  • Associated with (severe) bleeding - Can be reversed by vitamin K administration
60
Q

What does warfarin do?

A

Warfarin approved as anticoagulant drug. Mechanism of action discovered as inhibition of epoxide reductase.

61
Q

Thromcocytopenia/Thrombastenia

A

Acquired
• Leukaemia
Loss/dysfunction of platelets

  • Blood loss
  • Disseminated intravascular coagulation (DIC)
  • Drug-induced
  • Immune thrombocytopenic purpura (ITP)- don’t know the cause and produce antibodies against their platelets- never have a high platelet count to have a haemostatic response
62
Q

Inherited bleeding disorders- causes

A

Primary causes of inherited bleeding:

  • Platelet dysfunction
  • Coagulation factor deficiency or haemophilia (severe)
  • Thrombocytopenia (mild)
63
Q

Haemophilia A

A

Deficiency of FVIII
Cofactor for conversion of FX to FXa (intrinsic pathway)
Consolidation phase of thrombin generation
X-linked recessive
Female carrier, male offspring affected
Rare

64
Q

Haemophilia B

A

Deficiency of FIX
FIXa converts FX to FXa (intrinsic pathway)
Consolidation phase of thrombin generation
X-linked recessive
Female carrier, male offspring affected
Rare

65
Q

Von Willebrand Disease

A
  • Deficiency of vWF
  • Most common inherited bleeding disorder
  • Type 1 – heterozygous disease (autosomal dominant)
  • Type 2 – functional deficiency (autosomal dominant)
  • Type 3 – complete deficiency (autosomal recessive)
  • Platelet type: mutation in GP1 – bleeding severity is dependent on type
66
Q

Thrombosis

A

Involves the formation of a blood clot inside the vessel, blocking blood circulation

67
Q

Differences between the vein and artery

A 
Vein- Large diameter
Thin wall
Thin tunica media
Low pressure
Valves

More to do with blood pooling

Artery- Small diameter
Thick wall
Thick tunica media
High pressure
No valves

More to do with damage

68
Q

Main thrombotic disorders

A

Arterial thrombosis:

1) Myocardial infarction (MI; heart)
2) Atrial fibrillation (AF; heart)
3) Peripheral vascular disease (PVD; leg)
4) Stroke (brain)

Venous thrombosis:

1) Deep vein thrombosis (DVT; arm/leg)
2) Pulmonary embolism (PE; lungs)

69
Q

Arterial thrombosis- myocardial infarction and stroke- causes and events?

A
  • Caused by atherosclerosis: inflammation of the vessel wall with infiltration of macrophages (> foam cells) and fat deposits > Atherosclerotic plaque
  • Triggered by rupture of the atherosclerotic plaque
  • Precipitating event in myocardial infarction and ischaemic stroke
  • Thrombus is platelet-rich (as opposed to RBC and fibrin rich in venous thrombosis)
  • Uncontrolled platelet reaction
70
Q

Key risk factors of arterial thrombosis- same as atherosclerosis

A
  • Advanced age
  • Smoking
  • Diabetes
  • Hypertension
  • Cholesterol
  • Poor diet
  • Lack of exercise
  • Ethnicity
71
Q

Phases of a thrombotic response

A
  • Plaque fissure or rupture
  • Adhesion and activation of platelets
  • Activation of coagulation cascade
72
Q

Atherosclerotic plaque rupture

A

Progressive inflammatory disorder characterised by deposition of lipids, oxidative stress.
With time, plaques rupture and induce thrombotic events.
Atherosclerotic plaques leads to local distances in blood flow, cellular dysfunction.
Atherothrombotic event leads focal necrosis of cardiac tissue.
Heart becomes so damaged leading to cardiac arrest.

73
Q

Arterial thrombosis- Primary haemostatic response

A
  • Platelets bind to collagen
  • Adhesion and activation
  • Release of pro-aggregatory substances ADP, TxA2
  • Autocatalytic expansion of thrombus
  • Controlled by endothelial NO and PGI2
74
Q

Arterial thrombosis- Thrombotic response

A
  • Platelets bind to collagen and exposed to oxidised lipids from plaques
  • Activation
  • Release of proaggregatory substances ADP, TxA2
  • Autocatalytic expansion of thrombus
  • Reduced bioavailability of endothelial NO and production of PGI2
  • Occlusive thrombi
75
Q

Treatment of atherothrombosis

A

Antiplatelets
– Aspirin (inhibition of COX-1 and thromboxane production)- stops platelet activation
– Anti aIIbb3 (receptor for fibrinogen and vWF)
• Abciximab, Tirofiban
– Anti P2Y (receptor for ADP induced platelet aggregation)
• Clopidogrel, Ticagrelor, Prasugrel

Fibrinolytics (tPA/uPA derivatives)

76
Q

Venous thrombosis- deep vein thrombosis and pulmonary embolism

A

Venous thrombosis is caused by stasis and coagulation imbalance.

77
Q

Venous Thrombosis-DVT

A
  • Occurs under low blood flow as opposed to arterial thrombosis which occurs under high flow, develops around valves (more turbulent flow)
  • Less complex phenotype than arterial thrombosis, determined by coagulibility of blood
  • Thrombus is fibrin and erythrocyte rich

Clot puts pressure on endothelial cells and become leaky and escape and accumulate in other spaces outside the tube.

78
Q

Venous thrombosis- risk factors

A 
•	Immobilisation
•	Surgery 
•	Cancer
•	Pregnancy
•	Oral contraceptives
•	Genetic risk factors: 
	-Deficiencies in coagulation inhibitors
	-Factor V Leiden mutation
79
Q

Venous thrombosis-Pulmonary embolism (PE)

A
  • DVT or part of it breaks off from vein
  • Break away clot travels through bloodstream to heart and lungs
  • Clot blocks vessel in lung interrupting blood supply
80
Q

Treatment for PE

A

Immediate onset of anticoagulant effect:
– Unfractionated Heparin (intravenous – helps antithrombin to inhibit thrombin and Xa)
– Low Molecular Weight Heparin (LMWH; subcutaneous)
Slow onset:
– VKA, monitored by INR

Direct thrombin inhibitors (Dabigatran) promising in clinical trials.

IMS (13 decks)

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